Role of Regulators of G-Protein Signaling 4 in Ca2+ Signaling in Mouse Pancreatic Acinar Cells.
10.4196/kjpp.2011.15.6.383
- Author:
Soonhong PARK
1
;
Syng Ill LEE
;
Dong Min SHIN
Author Information
1. Department of Oral Biology, Yonsei University College of Dentistry, Seoul 120-752, Korea. dmshin@yuhs.ac
- Publication Type:Original Article
- Keywords:
RGS4;
Ca2+ signaling;
Pancreatic acinar cells
- MeSH:
Acinar Cells;
Amylases;
Animals;
Calcium-Transporting ATPases;
GTP Phosphohydrolases;
GTP-Binding Proteins;
Mice;
Pancreas;
Proteins;
Receptors, Muscarinic;
Reticulum;
RGS Proteins
- From:The Korean Journal of Physiology and Pharmacology
2011;15(6):383-388
- CountryRepublic of Korea
- Language:English
-
Abstract:
Regulators of G-protein signaling (RGS) proteins are regulators of Ca2+ signaling that accelerate the GTPase activity of the G-protein alpha-subunit. RGS1, RGS2, RGS4, and RGS16 are expressed in the pancreas, and RGS2 regulates G-protein coupled receptor (GPCR)-induced Ca2+ oscillations. However, the role of RGS4 in Ca2+ signaling in pancreatic acinar cells is unknown. In this study, we investigated the mechanism of GPCR-induced Ca2+ signaling in pancreatic acinar cells derived from RGS4-/- mice. RGS4-/- acinar cells showed an enhanced stimulus intensity response to a muscarinic receptor agonist in pancreatic acinar cells. Moreover, deletion of RGS4 increased the frequency of Ca2+ oscillations. RGS4-/- cells also showed increased expression of sarco/endoplasmic reticulum Ca2+ ATPase type 2. However, there were no significant alterations, such as Ca2+ signaling in treated high dose of agonist and its related amylase secretion activity, in acinar cells from RGS4-/- mice. These results indicate that RGS4 protein regulates Ca2+ signaling in mouse pancreatic acinar cells.
